In the human peripheral circulatory system, veins in the leg work against gravity and pump blood towards the heart. Healthy function of venous anatomy depends strongly on a series of one-way valves that open and close, with assistance from the venous pump, a collection of skeletal muscles that aid in the circulation of blood by muscle contractions; the valves act as one-way pressure regulators to negate the effects of gravity-induced hydrostatic blood pressure, especially in the standing position where pressures of over 90 mm Hg can be experienced. When the peripheral venous system does not function properly a condition known as venous insufficiency or over a long-term, chronic venous insufficiency or CVI develops.
CVI results from either venous valve dysfunction and blood reflux; or venous obstruction due to thrombosis; or a combination of both. Venous valve reflux causes stagnant blood to pool in the leg leading to fluid/blood cell leakage into the skin and other tissues. Venous valve dysfunction is caused either primarily by congenitally weak valves; or secondarily by direct trauma, thrombosis, hormonal changes (e.g. pregnancy), and/or prolonged standing or sitting. The condition is diagnosed through physical examination, venous duplex ultrasonography, and venous air plethysmography, or less commonly by contrast venography.
CVI can manifest itself in both superficial and deep veins. Since a superficial vein is not paired with an artery, CVI in a superficial vein typically has minor health implications and can be more readily treated or removed without concern for circulatory health. A deep vein is well beneath the skin and is paired with an artery. These paired veins carry most of the blood in the body, and given their importance to circulation, are not typically removed. The risks related to untreated CVI are severe and include major injury and death from deep vein thrombosis (DVT); DVT is the formation of a blood clot in deep veins typically in the legs, thighs, or pelvis. In mild cases, CVI may cause chronic itchy skin, slight pain and swelling; in moderate to severe cases, CVI may cause lifestyle interfering edema, ulcerations and infections (cellulitis, lymphangitis).
Current CVI treatments for dysfunctional valves range from surgical reconstruction of valves to endovascular (catheter-based) technologies. Surgical correction of refluxing valves is complicated and expensive. Long-term outcomes are unpredictable and procedural risks are high. Endovascular alternatives to surgery such as venoplasty ballooning, catheter-directed lysis, and stent implantation have advanced rapidly. Although these new catheter-based techniques provide simplified treatment, their best outcomes are limited to recanalization of the vein, not minimizing venous reflux or reversing the long-term symptoms of CVI and acute DVT.
Early attempts at developing a prosthetic venous valve often led to tilting of the valve, thrombus formation at the valve, continued reflux from leaflet thickening or other problems after the valve was delivered.